Signal transduction through decay-accelerating factor. Interaction of glycosyl-phosphatidylinositol anchor and protein tyrosine kinases p56lck and p59fyn 1.

作者: A S Shaw , T Fujita , J Kwong , M W Olszowy , A M Shenoy-Scaria

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摘要: Decay-accelerating factor (DAF or CD55) is a 70-kDa glycosyl-phosphatidylinositol (GPI)-anchored protein that protects cells from complement-mediated lysis by either preventing the formation of dissociating C3 convertases. Cross-linking DAF on human peripheral T polyclonal antibodies has previously been reported to lead lymphocyte proliferation. Two mAb, both mapping third short consensus repeat region DAF, were able trigger proliferation cells. To determine role GPI anchor in cell activation, we transfected EL-4 murine thymoma with cDNA encoding transmembrane form (DAF-TM). The DAF-transfected transduce late activation events as evidenced IL-2 production, whereas DAF-TM unable do so. GPI-anchored was early leading tyrosine phosphorylation 40-kDa and several proteins 85-95 kDa range--an event absent DAF-TM-transfected Furthermore, anti-DAF immunoprecipitates contain kinase activity 40-, 56-60-, 85-kDa proteins, did not have an associated activity. Both p56lck p59fyn In HeLa fyn, p59fyn. This complex src family kinases requires suggests pathway for signaling through membrane proteins.

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